一組荷蘭科研人員已經(jīng)證明了一點(diǎn)熱量可以在很大程度上讓某些類型的癌癥療法增效,。一些臨床醫(yī)生使用局部體溫過高（讓腫瘤升溫到41-43攝氏度，即大約106-109華氏度）的方法增加某些癌癥療法的療效,，諸如放射性療法和化學(xué)療法,。然而，迄今為止科研人員不清楚體溫過高如何起到了幫助作用,。Przemek M. Krawczyk及其同事證明了體溫過高阻斷了一種關(guān)鍵的DNA修復(fù)路徑,，如果沒有體溫過高，這種修復(fù)路徑就會(huì)妨礙放射性療法和化學(xué)療法,，溫度增加導(dǎo)致了在DNA修復(fù)中起到關(guān)鍵作用的BRCA2蛋白降解,，并且讓放射性療法和化學(xué)療法更有效地阻止腫瘤生長(zhǎng)。目前,，能夠抑制PARP-1酶（這是另一種參與DNA修復(fù)的蛋白）的藥物正在被用于治療BRCA基因沒有激活的罕見癌癥,。這組作者說，體溫過高是一種非侵入性,、非毒性的工具,，可能有助于改善PARP-1抑制劑的效果，而且還可能改善與正常的BRCA基因有關(guān)的其他癌癥的當(dāng)前療法的效果,。（生物谷Bioon.com）
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.1101053108
Mild hyperthermia inhibits homologous recombination, induces BRCA2 degradation, and sensitizes cancer cells to poly (ADP-ribose) polymerase-1 inhibition
Przemek M. Krawczyka,1, Berina Eppinkb,1, Jeroen Essersb,c,d,1, Jan Stapa,1, Hans Rodermonde, Hanny Odijkb, Alex Zelenskyb, Chris van Breee, Lukas J. Stalpersf, Marrije R. Buistg, Thomas Soulliéh, Joost Rensh, Hence J. M. Verhagend, Mark J. O'Connori, Nicolaas A. P. Frankene,f, Timo L. M. ten Hagenh, Roland Kanaarb,c,2, and Jacob A. Atena
Abstract
Defective homologous recombination (HR) DNA repair imposed by BRCA1 or BRCA2 deficiency sensitizes cells to poly (ADP-ribose) polymerase (PARP)-1 inhibition and is currently exploited in clinical treatment of HR-deficient tumors. Here we show that mild hyperthermia (41–42.5 °C) induces degradation of BRCA2 and inhibits HR. We demonstrate that hyperthermia can be used to sensitize innately HR-proficient tumor cells to PARP-1 inhibitors and that this effect can be enhanced by heat shock protein inhibition. Our results, obtained from cell lines and in vivo tumor models, enable the design of unique therapeutic strategies involving localized on-demand induction of HR deficiency, an approach that we term induced synthetic lethality.
